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Article ; Online: Regulation of innate immune signaling pathways by autophagy in dengue virus infection.

Wan, Shu-Wen / Lee, Ying-Ray / Ho, Tzong-Shiann / Chang, Chih-Peng

2021 Volume 74, Issue 2, Page(s) 170–179

Abstract: Autophagy is not only an intracellular recycling degradation system that maintains cellular homeostasis but is also a component of innate immunity that contributes to host defense against viral infection. The viral components as well as viral particles ... ...

Abstract	Autophagy is not only an intracellular recycling degradation system that maintains cellular homeostasis but is also a component of innate immunity that contributes to host defense against viral infection. The viral components as well as viral particles trapped in autophagosomes can be delivered to lysosomes for degradation. Abundant evidence indicates that dengue virus (DENV) has evolved the potent ability to hijack or subvert autophagy process for escaping host immunity and promoting viral replication. Moreover, autophagy is often required to deliver viral components to pattern recognition receptors signaling for interferon (IFN)-mediated viral elimination. Hence, this review summarizes DENV-induced autophagy, which exhibits dual effects on proviral activity of promoting replication and antiviral activity to eliminating viral particles.
MeSH term(s)	Autophagy ; Dengue/genetics ; Dengue Virus ; Humans ; Immunity, Innate ; Signal Transduction ; Virus Diseases ; Virus Replication
Language	English
Publishing date	2021-09-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1492141-8
ISSN	1521-6551 ; 1521-6543
ISSN (online)	1521-6551
ISSN	1521-6543
DOI	10.1002/iub.2554
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Article ; Online: Honokiol Suppresses Cell Proliferation and Tumor Migration through ROS in Human Anaplastic Thyroid Cancer Cells.

Liao, Kai-Sheng / Lee, Ying-Ray / Chao, Wen-Ying / Huang, Yen-Ju / Chung, Hui-Chen / Chen, Shu-Hsin / Li, Yi-Zhen / Zhao, Pei-Wen / Chang, Hong-Yi

Endocrine, metabolic & immune disorders drug targets

2024

Abstract: Background: Honokiol is a natural polyphenolic compound extracted from Magnolia officinali, which is commonly used material in Chinese herbal medicine, has a variety of biological functions, including anti-tumor, anti-oxidant, anti-inflammation, anti- ... ...

Abstract	Background: Honokiol is a natural polyphenolic compound extracted from Magnolia officinali, which is commonly used material in Chinese herbal medicine, has a variety of biological functions, including anti-tumor, anti-oxidant, anti-inflammation, anti-microbial and anti-allergy. Although honokiol has numerous beneficial effects on human diseases, the underlying mechanisms of tumor metastasis are still unclear. Previously, we reported that honokiol suppresses thyroid cancer cell proliferation with cytotoxicity through cell cycle arrest, apoptosis, and dysregulation of intracellular hemostasis. Herein, we hypothesized that the antioxidant effect of honokiol might play a critical role in thyroid cancer cell proliferation and migration. Methods: The cell viability assays, cellular reactive oxygen species (ROS) activity, cell migration, and immunoblotting were performed after cells were treated with honokiol. Results: Based on this hypothesis, we first demonstrated that honokiol suppresses cell proliferation in two human anaplastic thyroid carcinoma (ATC) cell lines, KMH-2 and ASH-3, within a dosage- and time-dependent manner by cell counting kit-8 (CCK-8) assay. Next, we examined that honokiol induced ROS activation and could be suppressed by pre-treated with an antioxidant agent, N-acetyl-l-cysteine (NAC). Furthermore, the honokiol suppressed cell proliferation can be rescued by pre-treated with NAC. Finally, we demonstrated that honokiol inhibited ATC cell migration by modulating epithelial-mesenchymal transition (EMT)-related markers by Western blotting. Conclusion: Taken together, we provided the potential mechanism for treating ATC cells with honokiol, which significantly suppresses tumor proliferation and inhibits tumor metastasis in vitro through reactive oxygen species (ROS) induction.
Language	English
Publishing date	2024-04-24
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2228325-0
ISSN	2212-3873 ; 1871-5303
ISSN (online)	2212-3873
ISSN	1871-5303
DOI	10.2174/0118715303295608240408082523
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Article ; Online: Piperlongumine Induces Cellular Apoptosis and Autophagy via the ROS/Akt Signaling Pathway in Human Follicular Thyroid Cancer Cells.

Lin, Tsung-Hsing / Kuo, Chin-Ho / Zhang, Yi-Sheng / Chen, Pin-Tzu / Chen, Shu-Hsin / Li, Yi-Zhen / Lee, Ying-Ray

International journal of molecular sciences

2023 Volume 24, Issue 9

Abstract: Thyroid cancer (TC) is the most common endocrine malignancy. Recently, the global incidence of TC has increased rapidly. Differentiated thyroid cancer includes papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC), which are the most ... ...

Abstract	Thyroid cancer (TC) is the most common endocrine malignancy. Recently, the global incidence of TC has increased rapidly. Differentiated thyroid cancer includes papillary thyroid carcinoma (PTC) and follicular thyroid carcinoma (FTC), which are the most common types of TC. Although PTCs and FTCs exert good prognoses and high survival rates, FTCs tend to be more aggressive than PTCs. There is an urgent need to improve patient outcomes by developing effective therapeutic agents for FTCs. Piperlongumine exerts anti-cancer effects in various human carcinomas, including human anaplastic TCs and PTCs. However, the anti-cancer effects of piperlongumine in FTCs and the underlying mechanisms are yet to be elucidated. Therefore, in the present study, we evaluated the effect of piperlongumine on cell proliferation, cell cycle, apoptosis, and autophagy in FTC cells with flowcytometry and Western blot. We observed that piperlongumine caused growth inhibition, cell cycle arrest, apoptosis induction, and autophagy elevation in FTC cells. Activities of reactive oxygen species and the downstream PI3K/Akt pathway were the underlying mechanisms involved in piperlongumine mediated anti-FTC effects. Advancements in our understanding of the effects of piperlongumine in FTC hold promise for the development of novel therapeutic strategies.
MeSH term(s)	Humans ; Proto-Oncogene Proteins c-akt/metabolism ; Reactive Oxygen Species/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Adenocarcinoma, Follicular/pathology ; Signal Transduction ; Thyroid Neoplasms/pathology ; Apoptosis ; Autophagy
Chemical Substances	Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Reactive Oxygen Species ; piperlongumine (SGD66V4SVJ) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-)
Language	English
Publishing date	2023-04-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24098048
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Article ; Online: FAK Executes Anti-Senescence via Regulating EZH2 Signaling in Non-Small Cell Lung Cancer Cells

Hsiang-Hao Chuang / Ming-Shyan Huang / Yen-Yi Zhen / Cheng-Hao Chuang / Ying-Ray Lee / Michael Hsiao / Chih-Jen Yang

Biomedicines, Vol 10, Iss 8, p

2022 Volume 1937

Abstract: Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase overexpressed in various cancer types that plays a critical role in tumor progression. Accumulating evidence suggests that targeting FAK, either alone or in combination with other agents, may ... ...

Abstract	Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase overexpressed in various cancer types that plays a critical role in tumor progression. Accumulating evidence suggests that targeting FAK, either alone or in combination with other agents, may serve as an effective therapeutic strategy for numerous cancers. In addition to retarding proliferation, metastasis, and angiogenesis, FAK inhibition triggers cellular senescence in lung cancer cells. However, the detailed mechanism remains enigmatic. In the present study, we found that FAK inhibition not only elicits DNA-damage signaling but also downregulates enhancer of zeste homolog 2 (EZH2) expression. The manipulation of FAK expression influences EZH2 expression and corresponding signaling in vitro. Immunohistochemistry shows that active FAK signaling corresponds with the activation of the EZH2-mediated signaling cascade in lung-cancer-cells-derived tumor tissues. We also found that ectopic EZH2 expression attenuates FAK-inhibition-induced cellular senescence in lung cancer cells. Our results identify EZH2 as a critical downstream effector of the FAK-mediated anti-senescence pathway. Targeting FAK-EZH2 axis-induced cellular senescence may represent a promising therapeutic strategy for restraining tumor growth.
Keywords	FAK ; EZH2 ; senescence ; lamin A/C ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-08-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Ivermectin induces cell cycle arrest and caspase-dependent apoptosis in human urothelial carcinoma cells.

Tung, Chun-Liang / Chao, Wen-Ying / Li, Yi-Zhen / Shen, Cheng-Huang / Zhao, Pei-Wen / Chen, Shu-Hsin / Wu, Tzu-Yun / Lee, Ying-Ray

International journal of medical sciences

2022 Volume 19, Issue 10, Page(s) 1567–1575

Abstract: Bladder carcinoma is one of the most common malignancies worldwide, and >90% of all bladder cancers are classified as urothelial carcinomas (UC). Surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy are evidence-based treatments that ... ...

Abstract	Bladder carcinoma is one of the most common malignancies worldwide, and >90% of all bladder cancers are classified as urothelial carcinomas (UC). Surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy are evidence-based treatments that are administered depending on the clinical stage of UC. All these treatments exhibited limited effects in cases of metastatic UC, and UC with specific location, invasiveness, and recurrence. Therefore, a new therapeutic strategy for UC is urgently needed. Ivermectin, an avermectin derivative, has been reported to be effective against various parasites, and its pharmacokinetic and pharmacodynamic properties as well as safety are well understood in humans. Recently, ivermectin was shown to exhibit therapeutic benefits against various virus infections
MeSH term(s)	Apoptosis ; Carcinoma, Transitional Cell ; Caspases ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Ivermectin/pharmacology ; Ivermectin/therapeutic use ; JNK Mitogen-Activated Protein Kinases ; Urinary Bladder Neoplasms/pathology
Chemical Substances	Ivermectin (70288-86-7) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Caspases (EC 3.4.22.-)
Language	English
Publishing date	2022-09-11
Publishing country	Australia
Document type	Journal Article
ZDB-ID	2151424-0
ISSN	1449-1907 ; 1449-1907
ISSN (online)	1449-1907
ISSN	1449-1907
DOI	10.7150/ijms.76623
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Article ; Online: RNA Interference Approach Is a Good Strategy against SARS-CoV-2.

Lee, Ying-Ray / Tsai, Huey-Pin / Yeh, Chun-Sheng / Fang, Chiung-Yao / Chan, Michael W Y / Wu, Tzu-Yun / Shen, Cheng-Huang

Viruses

2022 Volume 15, Issue 1

Abstract: COVID-19, caused by SARS-CoV-2, created a devastating outbreak worldwide and consequently became a global health concern. However, no verifiable, specifically targeted treatment has been devised for COVID-19. Several emerging vaccines have been used, but ...

Abstract	COVID-19, caused by SARS-CoV-2, created a devastating outbreak worldwide and consequently became a global health concern. However, no verifiable, specifically targeted treatment has been devised for COVID-19. Several emerging vaccines have been used, but protection has not been satisfactory. The complex genetic composition and high mutation frequency of SARS-CoV-2 have caused an uncertain vaccine response. Small interfering RNA (siRNA)-based therapy is an efficient strategy to control various infectious diseases employing post-transcriptional gene silencing through the silencing of target complementary mRNA. Here, we designed two highly effective shRNAs targeting the conserved region of RNA-dependent RNA polymerase (RdRP) and spike proteins capable of significant SARS-CoV-2 replication suppression. The efficacy of this approach suggested that the rapid development of an shRNA-based therapeutic strategy might prove to be highly effective in treating COVID-19. However, it needs further clinical trials.
MeSH term(s)	Humans ; COVID-19/therapy ; RNA Interference ; RNA, Small Interfering/genetics ; RNA-Dependent RNA Polymerase/genetics ; RNA-Dependent RNA Polymerase/metabolism ; SARS-CoV-2/genetics ; SARS-CoV-2/metabolism
Chemical Substances	RNA, Small Interfering ; RNA-Dependent RNA Polymerase (EC 2.7.7.48)
Language	English
Publishing date	2022-12-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v15010100
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Article: FAK Executes Anti-Senescence via Regulating EZH2 Signaling in Non-Small Cell Lung Cancer Cells.

Chuang, Hsiang-Hao / Huang, Ming-Shyan / Zhen, Yen-Yi / Chuang, Cheng-Hao / Lee, Ying-Ray / Hsiao, Michael / Yang, Chih-Jen

Biomedicines

2022 Volume 10, Issue 8

Abstract	Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase overexpressed in various cancer types that plays a critical role in tumor progression. Accumulating evidence suggests that targeting FAK, either alone or in combination with other agents, may serve as an effective therapeutic strategy for numerous cancers. In addition to retarding proliferation, metastasis, and angiogenesis, FAK inhibition triggers cellular senescence in lung cancer cells. However, the detailed mechanism remains enigmatic. In the present study, we found that FAK inhibition not only elicits DNA-damage signaling but also downregulates enhancer of zeste homolog 2 (EZH2) expression. The manipulation of FAK expression influences EZH2 expression and corresponding signaling in vitro. Immunohistochemistry shows that active FAK signaling corresponds with the activation of the EZH2-mediated signaling cascade in lung-cancer-cells-derived tumor tissues. We also found that ectopic EZH2 expression attenuates FAK-inhibition-induced cellular senescence in lung cancer cells. Our results identify EZH2 as a critical downstream effector of the FAK-mediated anti-senescence pathway. Targeting FAK-EZH2 axis-induced cellular senescence may represent a promising therapeutic strategy for restraining tumor growth.
Language	English
Publishing date	2022-08-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10081937
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Article ; Online: Regulation of autophagy, glucose uptake, and glycolysis under dengue virus infection

Ying‐Ray Lee / Shan‐Ying Wu / Ruei‐Yi Chen / Yee‐Shin Lin / Trai‐Ming Yeh / Hsiao‐Sheng Liu

Kaohsiung Journal of Medical Sciences, Vol 36, Iss 11, Pp 911-

2020 Volume 919

Abstract: Abstract We previously reported that dengue virus (DENV)‐induced autophagy plays a promoting role in viral replication and pathogenesis both in vitro and in vivo. Although it is known that DENV infection increases glycolysis, which promotes viral ... ...

Abstract	Abstract We previously reported that dengue virus (DENV)‐induced autophagy plays a promoting role in viral replication and pathogenesis both in vitro and in vivo. Although it is known that DENV infection increases glycolysis, which promotes viral replication, the role of glucose metabolism together with autophagic activity in DENV replication remains unclear. In this study, we reveal that DENV2 infection increased autophagic activity, glucose uptake, protein levels of glucose transporter‐1 (GLUT1), and glycolysis rate‐limiting enzyme hexokinase‐2 (HK2) in cells. Furthermore, the protein levels of LC3‐II and HK2 were increased in the brain tissues of the DENV2‐infected suckling mice. However, DENV2 infection decreased ATP level and showed no effect on mRNA expression of HK2 and phosphofructokinase, as well as lactate production, indicating that DENV2‐regulated glycolytic flux occurs at the post‐transcriptional level and is lactate pathway‐independent. Moreover, amiodarone‐induced autophagic activity, glucose uptake, HK2 level, and viral titer were reversed by the autophagy inhibitor spautin‐1 or silencing of Atg5 gene expression. Intriguingly, blocking of glycolysis, HK2 protein level, and viral titer were accordingly decreased, but autophagic activity was increased, suggesting the existence of another regulation mechanism that influences the relationship between glycolysis and autophagy. This is the first report to reveal that DENV2‐induced autophagy positively regulates glycolysis and viral replication in vitro and in vivo. Our findings open a new avenue wherein metabolic modulation could be used as a target for the treatment of DENV infection.
Keywords	autophagy ; dengue virus ; glucose uptake ; glycolysis ; Medicine (General) ; R5-920
Subject code	570
Language	English
Publishing date	2020-11-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Secretory autophagy promotes RAB37-mediated insulin secretion under glucose stimulation both

Wu, Shan-Ying / Wu, Hung-Tsung / Wang, Yi-Ching / Chang, Chih-Jen / Shan, Yan-Shen / Wu, Shang-Rung / Chiu, Yen-Chi / Hsu, Chia-Lang / Juan, Hsueh-Fen / Lan, Kai-Ying / Chu, Chi-Wen / Lee, Ying-Ray / Lan, Sheng-Hui / Liu, Hsiao-Sheng

Autophagy

2022 Volume 19, Issue 4, Page(s) 1239–1257

Abstract: High blood glucose is one of the risk factors for metabolic disease and INS (insulin) is the key regulatory hormone for glucose homeostasis. Hypoinsulinemia accompanied with hyperglycemia was diagnosed in mice with pancreatic β-cells exhibiting autophagy ...

Abstract	High blood glucose is one of the risk factors for metabolic disease and INS (insulin) is the key regulatory hormone for glucose homeostasis. Hypoinsulinemia accompanied with hyperglycemia was diagnosed in mice with pancreatic β-cells exhibiting autophagy deficiency; however, the underlying mechanism remains elusive. The role of secretory autophagy in the regulation of metabolic syndrome is gaining more attention. Our data demonstrated that increased macroautophagic/autophagic activity leads to induction of insulin secretion in β-cells both
MeSH term(s)	Animals ; Mice ; Autophagy/physiology ; Glucose/metabolism ; Insulin Secretion ; Proteomics ; rab GTP-Binding Proteins/metabolism ; Insulin/metabolism ; Hyperglycemia/metabolism ; Insulin-Secreting Cells/metabolism
Chemical Substances	Glucose (IY9XDZ35W2) ; rab GTP-Binding Proteins (EC 3.6.5.2) ; Insulin
Language	English
Publishing date	2022-09-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2022.2123098
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Article ; Online: Regulation of autophagy, glucose uptake, and glycolysis under dengue virus infection.

Lee, Ying-Ray / Wu, Shan-Ying / Chen, Ruei-Yi / Lin, Yee-Shin / Yeh, Trai-Ming / Liu, Hsiao-Sheng

The Kaohsiung journal of medical sciences

2020 Volume 36, Issue 11, Page(s) 911–919

Abstract: We previously reported that dengue virus (DENV)-induced autophagy plays a promoting role in viral replication and pathogenesis both in vitro and in vivo. Although it is known that DENV infection increases glycolysis, which promotes viral replication, the ...

Abstract	We previously reported that dengue virus (DENV)-induced autophagy plays a promoting role in viral replication and pathogenesis both in vitro and in vivo. Although it is known that DENV infection increases glycolysis, which promotes viral replication, the role of glucose metabolism together with autophagic activity in DENV replication remains unclear. In this study, we reveal that DENV2 infection increased autophagic activity, glucose uptake, protein levels of glucose transporter-1 (GLUT1), and glycolysis rate-limiting enzyme hexokinase-2 (HK2) in cells. Furthermore, the protein levels of LC3-II and HK2 were increased in the brain tissues of the DENV2-infected suckling mice. However, DENV2 infection decreased ATP level and showed no effect on mRNA expression of HK2 and phosphofructokinase, as well as lactate production, indicating that DENV2-regulated glycolytic flux occurs at the post-transcriptional level and is lactate pathway-independent. Moreover, amiodarone-induced autophagic activity, glucose uptake, HK2 level, and viral titer were reversed by the autophagy inhibitor spautin-1 or silencing of Atg5 gene expression. Intriguingly, blocking of glycolysis, HK2 protein level, and viral titer were accordingly decreased, but autophagic activity was increased, suggesting the existence of another regulation mechanism that influences the relationship between glycolysis and autophagy. This is the first report to reveal that DENV2-induced autophagy positively regulates glycolysis and viral replication in vitro and in vivo. Our findings open a new avenue wherein metabolic modulation could be used as a target for the treatment of DENV infection.
MeSH term(s)	A549 Cells ; Amiodarone/pharmacology ; Animals ; Animals, Newborn ; Autophagy/drug effects ; Autophagy/genetics ; Autophagy-Related Protein 5/antagonists & inhibitors ; Autophagy-Related Protein 5/genetics ; Autophagy-Related Protein 5/metabolism ; Benzylamines/pharmacology ; Biological Transport ; Brain/metabolism ; Brain/pathology ; Brain/virology ; Chlorocebus aethiops ; Dengue/genetics ; Dengue/metabolism ; Dengue/pathology ; Dengue/virology ; Dengue Virus/genetics ; Dengue Virus/growth & development ; Dengue Virus/metabolism ; Gene Expression Regulation ; Glucose/metabolism ; Glucose Transporter Type 1/genetics ; Glucose Transporter Type 1/metabolism ; Glycolysis/drug effects ; Glycolysis/genetics ; Hexokinase/genetics ; Hexokinase/metabolism ; Host-Pathogen Interactions/genetics ; Humans ; Mice ; Mice, Inbred ICR ; Microtubule-Associated Proteins/genetics ; Microtubule-Associated Proteins/metabolism ; Phosphofructokinases/genetics ; Phosphofructokinases/metabolism ; Quinazolines/pharmacology ; Signal Transduction ; Vero Cells ; Virus Replication/drug effects ; Virus Replication/genetics
Chemical Substances	Atg5 protein, mouse ; Autophagy-Related Protein 5 ; Benzylamines ; Glucose Transporter Type 1 ; Map1lc3b protein, mouse ; Microtubule-Associated Proteins ; Quinazolines ; Slc2a1 protein, mouse ; spautin-1 ; Phosphofructokinases (EC 2.7.1 -) ; Hexokinase (EC 2.7.1.1) ; hexokinase 2, mouse (EC 2.7.1.1) ; Glucose (IY9XDZ35W2) ; Amiodarone (N3RQ532IUT)
Language	English
Publishing date	2020-08-12
Publishing country	China (Republic : 1949- )
Document type	Journal Article
ZDB-ID	639302-0
ISSN	2410-8650 ; 0257-5655
ISSN (online)	2410-8650
ISSN	0257-5655
DOI	10.1002/kjm2.12271
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